A 44-year-old male presents following an intentional overdose. His arterial blood gases (ABG) are presented below:
| Parameter |
Patient Value |
Adult Normal Range |
|
FiO2 |
0.21 |
|
|
pH |
7.36 |
7.35 – 7.45 |
|
pCO2 |
16.0 mmHg (2.13 kPa) * |
35.0 – 45.0 (4.60 – 6.00) |
|
pO2 |
111 mmHg (14.8 kPa) |
|
|
SpO2 |
97% |
|
|
Bicarbonate |
9.0 mmol/L* |
22.0 – 26.0 |
|
Base Excess |
-15.0 mmol/L* |
-2.0 – +2.0 |
|
Lactate |
25.0 mmol/L* |
0.5 – 1.6 |
|
Sodium |
150 mmol/L* |
135 – 145 |
|
Potassium |
4.5 mmol/L |
3.5 – 5.0 |
|
Chloride |
117 mmol/L* |
95 – 105 |
|
Glucose |
4.0 mmol/L |
3.5 – 6.0 |
a) Describe the acid base abnormalities. (40% marks)
His lactate as measured on ABG is 25 mm/L, but the result on a venous blood sample taken at the same time and measured in the laboratory is only 5 mmol/L.
b) What is the most likely diagnosis? Explain the mechanism of the differences in measured lactates.
(20% marks)
Not available.
How very exciting. This SAQ must have been sitting on somebody's desk for two decades now, waiting for its turn. Yes, reader, this is a case of the fabled lactate gap, described in loving detail by Bala Venkatesh in his 2002 grimoire, Data Interpretation in Critical Care Medicine. It goes without saying that all trainees should own this book, as it has been a source of countless weird metabolic problems and ABG interpretation questions. Interestingly (in case anybody is interested), the patient data in this SAQ are totally different to the ABG in Venkatesh's book (Question 1.12), but exactly the same as Question 20.2 from the second paper of 2017.
But first, a), the acid base abnormalities:
but, the lactate
Yes; the discrepancy between the lab lactate and the gas lactate is due to the lactate electrode being confused by the glycolic acid in this patient's bloodstream. The patient has obviously overdosed on ethylene glycol.
The amperometric measurement of lactate uses the lactate-sensitive electrode, relying on the use of lactate oxidase. This enzyme catalyses the reaction which converts lactate into pyruvate, producing hydrogen peroxide which is reduced at the measurement cathode. Glycolic acid, the metabolic byproduct of ethylene glycol metabolism, also acts as the substrate for this enzyme. Therefore, in ethylene glycol poisoning the lactate measurement by the blood gas analyser will be spuriously elevated. The formal lactate measurement by use of a lactate dehydrogenase enzyme assay will still yield a correct result. The difference between the "formal" and the ABG lactate is described as the "lactate gap", and is a well known phenomenon of ethylene glycol toxicity (eg. Marwick et al, 2012). Apart from paracetamol and isoniazid as other potential culprits, the Reference Manual for the local ABG analyser lists a large number of molecules which can potentially cause interference with lactate measurement- notably ascorbic acid, bilirubin, citrate, EDTA, ethanol, heparin, glucose, paracetamol, salicylate and urea.
Marwick, J., R. O. C. Elledge, and A. Burtenshaw. "Ethylene glycol poisoning and the lactate gap." Anaesthesia 67.3 (2012): 299-299.
Soghoian, Sari, et al. "Ethylene Glycol Toxicity Presenting with Non‐Anion Gap Metabolic Acidosis." Basic & clinical pharmacology & toxicology 104.1 (2009): 22-26.